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Does Previous Hepatitis B Exposure Increase Liver Cancer Risk?

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http://www.hivandhepatitis.com/2010_conference/aasld/docs/1214_2010_b.html

HIV and Hepatitis.com Coverage of the

61st Annual Meeting of the American Association for the Study of Liver Diseases

(AASLD 2010)

October 29 - November 2, 2010, Boston, MA

Does Previous Hepatitis B Exposure Increase Liver Cancer Risk?

SUMMARY: People who were previously exposed to hepatitis B virus (HBV) have

an increased likelihood of developing hepatocellular carcinoma (HCC) even if

they clear the virus, according to a study presented at the recent American

Association for the Study of Liver Diseases " Liver Meeting " (AASLD 2010) in

Boston. These results suggest that individuals with prior HBV exposure, as well

as those with chronic hepatitis B, could benefit from regular liver cancer

monitoring.

By Liz Highleyman

Tang and colleagues from Henry Ford Health System in Detroit conducted a

retrospective cohort study to explore the association between hepatitis B

serologic status and development of HCC among North American patients.

Prior prospective studies (primarily of Asian populations) have shown that

individuals with perinatally acquired chronic HBV infection who seroconvert and

lose hepatitis B surface antigen (HBsAg) -- generally considered a cure -- are

still at increased risk for hepatocellular carcinoma.

In this analysis, investigators assessed whether North American HBsAg negative

individuals who are positive for hepatitis B core (HBc) or core plus surface

(HBs) antibodies are similarly at increased risk for liver cancer.

The study included more than 34,000 adult patients of an integrated healthcare

system who were tested for hepatitis B between January 1995 and December 2008.

Participants were divided into 3 groups according to HBV status:

Negative: tested negative for both HBsAg and HBc antibodies (n = 28,719);

Previous exposure: tested HBsAg negative, but HBc, or HBc and HBs, antibody

positive (n = 5141);

Chronic hepatitis B: tested HBsAg positive and HBc positive or HBV DNA positive

(n = 404).

Information about HCC diagnosis was obtained from the health system cancer

registry. The researchers used logistic regression to evaluate the influence of

HBV status on development of HCC.

Results

In a univariate analysis, both the chronic hepatitis B and previous exposure

groups were more likely to develop HCC compared with the negative cohort (2.2%,

0.8%, and 0.2%, respectively).

The previous exposure cohort was older, on average, than the other 2 groups.

The chronic hepatitis B and previous exposure groups were also more likely to

have the following characteristics, compared with the negative group:

Asian: 6.4%, 2.4%, and 0.9%, respectively;

Male: 66.8%, 61.1%, and 49.5%, respectively;

HIV positive: 14.6%, 9.3%, and 1.6%, respectively.

In a multivariate analysis taking into account factors including sex, age,

race/ethnicity, HIV status, and diabetes, previous HBV exposure and chronic

hepatitis B were both strong and significant predictors of HCC:

Previous exposure vs negative: odds ratio (OR) 3.06;

Chronic hepatitis B vs previous exposure: OR 3.09;

Chronic hepatitis B vs negative: OR 3.084.

Race/ethnicity was not a significant predictive factor in any of these

analyses.

Based on these findings, the investigators concluded that, " Previous HBV

exposure confers an increased risk for the development of HCC compared to HBV

negative patients in a North American cohort. "

" Additional studies are needed to assess the role of HCC screening among select

populations with previous exposure to HBV, " they added.

Investigator affiliations: Departments of Gastroenterology, Henry Ford Health

System; Biostatistics and Research Epidemiology, Henry Ford Health System,

Detroit, MI.

12/14/10

Reference

J Tang, R Sharma, L Lamerato, and others. 1389: Does Previous Hepatitis B

Infection Increase the Risk for Hepatocellular Carcinoma? 61st Annual Meeting of

the American Association for the Study of Liver Diseases (AASLD 2010). Boston,

October 29-November 2, 2010. Abstract 1389.

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